Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

Skip to main content
Fig. 2 | Biological Procedures Online

Fig. 2

From: Recent Advances in Crimean-Congo Hemorrhagic Fever Virus Detection, Treatment, and Vaccination: Overview of Current Status and Challenges

Fig. 2

During the first step of attachment, the Crimean-Congo Hemorrhagic Fever Virus (CCHFV) enters the host cytoplasm by relying on clathrin-dependent and pH-dependent mechanisms, which occur in stages 2 and 3, respectively. Upon entering the cytoplasm, viral genomes convert into positive-sense mRNA via the action of the RdRP enzyme. This mRNA then triggers the translation process, leading to the synthesis of viral proteins. Furthermore, these proteins collaborate to generate fresh negative-sense viral genomes enveloped with NP and a bound L protein to commence replication upon infecting the subsequent cell (stage 4). The GPC is transported into the endoplasmic reticulum (ER) and undergoes proteolytic processing through the ER and Golgi apparatus. This processing results in the production of mature GP, as well as the accessory proteins MLD, NSm, and GP38. Recently generated genomes are enclosed inside enveloped particles and the virus emerges from the Golgi apparatus to be released via the secretory route (stage 5). Subsequently, newly formed viral particles are discharged to invade other cells, while GP160/85, MLD, and GP38 are also discharged outside the cells, although the outcome of this release remains uncertain (stage 6). CCHFV proteins not only promote viral multiplication but also inhibit host apoptosis and innate immune mechanisms. The CCHFV NP can impede the intrinsic process of apoptosis at a stage that has not yet. In contrast, the CCHFV NSs facilitate apoptosis by disrupting the mitochondrial membrane or the extrinsic apoptotic pathways. CCHFV may induce apoptosis by generating tumor necrosis factor (TNF) and activating the TNF death receptor pathway. The CCHFV NP is likewise cleaved by host caspase 3, however the presence of oligomeric conformations may hinder this cleavage process. The OTU domain of the CCHFV L protein inhibits the start of the type I interferon response by its deubiquitylating action, suppressing the RIG-I-dependent pathway. MAVS refers to the mitochondrial antiviral signaling protein, whereas vRNA stands for viral RNA [2]

Back to article page